Recent advances in the application of photodynamic therapy (PDT) are showing great potential in the treatment of infections involving localised bacterial growth. The killing of bacteria by PDT involves the use of a photosensitiser and low-level light for treating localised bacterial infections. During PDT, the photoactivated photosensitiser molecule can either transfer an electron to the neighbouring molecule (i.e. Type-I reaction), where the electron transfer reactions between the triplet state sensitizer and biomolecules result in the generation of several radical species which can cause cell damage, or by a type-II reaction, where the energy transfer from triplet state species to molecular oxygen produces singlet oxygen (1O2), a highly reactive species causing cell death.
The activation of photosensitizers in the presence of oxygen results in the production of reactive oxygen species, involving hydroxyl radicals, superoxides and singlet oxygen. The oxygen based free radicals, involved in the photo oxidised inactivation of microorganisms acts on multiple targets resulting in instantaneous killing. This aspect of PDT makes the selection of photoresistant microbial strain highly unlikely. Production of highly reactive singlet oxygen capable of destroying biomolecules has been identified as the principle agent causing bacterial killing.
WO 2006/135344 teaches a composition that comprises a mixture of glycerol, ethanol and water, preferably in the ratio 30:20:50 by volume. This composition enables the photosensitizer deep into the dentinal tubules and the anatomical complexities of the tooth, releases significantly high singlet oxygen when activated, better uptake by the bacterial cells with less tendency for surface aggregation and also causes more severe destruction of bacterial cells (membrane damage and DNA damage). Photosensitizer, when dissolved in this formulation, when used along with an oxygen carrier, which also acts as a liquid optical conduit (perfluorodecahydro naphthalene) is able to eliminate bacteria more significantly from the root canal system (George S and Kishen A, J Biomed Opt, 2007; George S and Kishen A, J. Endod., 2007). Although this approach is advantageous in inactivating short-span, i.e. 2 days to 1 week, biofilms, it was not able to inactivate matured long-span biofilms (Kishen A et al, J Biomed Mater Res A, 2006). The primary factors that make inactivation of biofilm bacteria difficult are: (1) limited photosensitizer diffusion into the biofilm structure, (2) lack of proper oxygen tension in the interior of the biofilm, and (3) difficulty in ensuring proper light propagation through biofilm due to scattering and absorption of light.
There is therefore a need in the art for an improved photosensitising composition which is able to inactivate matured long-span biofilms.